Abstract
The objective of this study was to assess the impact of murine recombinant IFN-γ and anti-IFN-γ monoclonal antibody on the BALB/c mice experimental model of lupus. BALB/c female mice were immunized with a human anti-DNA antibody that carries the 16/6 idiotype. These mice were divided into several therapeutic groups according to different treatment strategies; injection with mouse recombinant IFN-γ, anti-IFN-γ mAb, phosphate-buffered saline (PBS), irrelevant mouse IgG and control groups that were neither treated nor immunized with the human anti-DNA antibody. The administration of IFN-γ intensified the degree of clinical, histological and serological parameters in this model of BALB/c murine lupus. This immunomanipulation decreased the mice longevity. All the laboratory parameters reflected acceleration of the disease in the IFN-γ treated group as an elevated sedimentation rare, decreased white blood cell count and the development of massive proteinuria. One month after the boost injection, all the mice that were immunized with the anti-DNA antibody, developed high titers of autoantibodies; however, following an additional month, their levels declined in the IFN-γ treated group. These findings were in concordance with an increased glomerular deposition of immune complexes in the IFN-γ treated mice. IFN-γ upregulated the levels of IL-4 and increased the number of IL-4 and IL-6 secreting splenocytes. In conclusion IFN-γ, administration can aggravate the clinical and laboratory outcome of 16/6 id induced lupus in BALB/c mice.
| Original language | English |
|---|---|
| Pages (from-to) | 445-454 |
| Number of pages | 10 |
| Journal | Lupus |
| Volume | 7 |
| Issue number | 7 |
| DOIs | |
| Publication status | Published - 1998 |
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Keywords
- Cytokines
- IFN-γ
- Systemic lupus erythematosus
- Th1 cells
- Th2 cells
ASJC Scopus subject areas
- Rheumatology
- Immunology
Cite this
Immunomodulation of murine experimental SLE-like disease by interferon-γ. / Amital, H.; Levi, Y.; Blank, M.; Barak, V.; Langevitz, P.; Afek, A.; Nicoletti, F.; Kopolovic, J.; Gilburd, B.; Meroni, P. L.; Shoenfeld, Y.
In: Lupus, Vol. 7, No. 7, 1998, p. 445-454.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Immunomodulation of murine experimental SLE-like disease by interferon-γ
AU - Amital, H.
AU - Levi, Y.
AU - Blank, M.
AU - Barak, V.
AU - Langevitz, P.
AU - Afek, A.
AU - Nicoletti, F.
AU - Kopolovic, J.
AU - Gilburd, B.
AU - Meroni, P. L.
AU - Shoenfeld, Y.
PY - 1998
Y1 - 1998
N2 - The objective of this study was to assess the impact of murine recombinant IFN-γ and anti-IFN-γ monoclonal antibody on the BALB/c mice experimental model of lupus. BALB/c female mice were immunized with a human anti-DNA antibody that carries the 16/6 idiotype. These mice were divided into several therapeutic groups according to different treatment strategies; injection with mouse recombinant IFN-γ, anti-IFN-γ mAb, phosphate-buffered saline (PBS), irrelevant mouse IgG and control groups that were neither treated nor immunized with the human anti-DNA antibody. The administration of IFN-γ intensified the degree of clinical, histological and serological parameters in this model of BALB/c murine lupus. This immunomanipulation decreased the mice longevity. All the laboratory parameters reflected acceleration of the disease in the IFN-γ treated group as an elevated sedimentation rare, decreased white blood cell count and the development of massive proteinuria. One month after the boost injection, all the mice that were immunized with the anti-DNA antibody, developed high titers of autoantibodies; however, following an additional month, their levels declined in the IFN-γ treated group. These findings were in concordance with an increased glomerular deposition of immune complexes in the IFN-γ treated mice. IFN-γ upregulated the levels of IL-4 and increased the number of IL-4 and IL-6 secreting splenocytes. In conclusion IFN-γ, administration can aggravate the clinical and laboratory outcome of 16/6 id induced lupus in BALB/c mice.
AB - The objective of this study was to assess the impact of murine recombinant IFN-γ and anti-IFN-γ monoclonal antibody on the BALB/c mice experimental model of lupus. BALB/c female mice were immunized with a human anti-DNA antibody that carries the 16/6 idiotype. These mice were divided into several therapeutic groups according to different treatment strategies; injection with mouse recombinant IFN-γ, anti-IFN-γ mAb, phosphate-buffered saline (PBS), irrelevant mouse IgG and control groups that were neither treated nor immunized with the human anti-DNA antibody. The administration of IFN-γ intensified the degree of clinical, histological and serological parameters in this model of BALB/c murine lupus. This immunomanipulation decreased the mice longevity. All the laboratory parameters reflected acceleration of the disease in the IFN-γ treated group as an elevated sedimentation rare, decreased white blood cell count and the development of massive proteinuria. One month after the boost injection, all the mice that were immunized with the anti-DNA antibody, developed high titers of autoantibodies; however, following an additional month, their levels declined in the IFN-γ treated group. These findings were in concordance with an increased glomerular deposition of immune complexes in the IFN-γ treated mice. IFN-γ upregulated the levels of IL-4 and increased the number of IL-4 and IL-6 secreting splenocytes. In conclusion IFN-γ, administration can aggravate the clinical and laboratory outcome of 16/6 id induced lupus in BALB/c mice.
KW - Cytokines
KW - IFN-γ
KW - Systemic lupus erythematosus
KW - Th1 cells
KW - Th2 cells
UR - http://www.scopus.com/inward/record.url?scp=7844221012&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=7844221012&partnerID=8YFLogxK
U2 - 10.1191/096120398678920406
DO - 10.1191/096120398678920406
M3 - Article
C2 - 9796846
AN - SCOPUS:7844221012
VL - 7
SP - 445
EP - 454
JO - Lupus
JF - Lupus
SN - 0961-2033
IS - 7
ER -